The effect of insulinopenic diabetes on the expression of glucose transporters in the small intestine was investigated. Enterocytes were sequentially isolated from jejunum and ileum of normal fed rats, streptozotocin-diabetic rats, and diabetic rats treated with insulin. Facilitative glucose transporter (GLUT) 2, GLUT5, and sodium-dependent glucose transporter 1 protein content was increased from 1.5-to 6-fold in enterocytes isolated from diabetic animals in both jejunum and ileum. Insulin was able to reverse the increase in transporter protein expression seen after induction of diabetes.There was a four-to eightfold increase in the amount of enterocyte glucose transporter mRNA after diabetes with greater changes in sodium-dependent glucose transporter 1 and GLUT2 than in GLUT5 levels. In situ hybridization showed that after the induction of diabetes there was new hybridization in lower villus and crypt enterocytes that was reversed by insulin treatment.Thus, the increase in total hexose transport caused by diabetes is due to a premature expression of hexose transporters by enterocytes along the crypt-villus axis, causing a cumulative increase in enterocyte transporter protein during maturation. These changes are likely to represent an adaptive response by the organism to increase nutrient absorption in a perceived state of tissue starvation. These adaptive changes may lead to exacerbation of hyperglycemia in uncontrolled diabetes. (J.

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Reported gastrointestinal neoplasms in nonhuman primates are reviewed, and the clinical and pathologic features of 11 new cases are described. The 11 monkeys had a total of 12 malignant gastrointestinal neoplasms; one had two primary carcinomas, one in the colon and one in the duodenum. Ten of the 12 tumors were adenocarcinomas: two in the duodenum, one in the jejunum, four in the distal ileum or region of the ileocecal valve and three in the large intestine. The remaining two lesions were a histiocytic lymphosarcoma of the stomach and a poorly differentiated sarcoma of the cecum. The 11 animals included nine Macaca mulatta, one Saguinus oedipus oedipus and one Galago crassicaudatus. All were adults and most were aged. There were six females and five males. Clinical signs included progressive weight loss, a palpable abdominal mass and intermittent diarrhea. Grossly, five of the adenocarcinomas were annular, and constricted the intestinal lumen. Microscopically, the carcinomas generally were well differentiated, and two produced mucin in quantities warranting the modifier "mucinous" adenocarcinoma. All tumors were locally invasive and six of nine monkeys with carcinomas had metastases, with the regional lymph nodes the principal site of involvement.

Abstract. A 6-year retrospective study o f necropsy material from a colony o f 200 gibbons showed strongyloidiasis to be the most frequent cause of death (24 cases). Clinical signs included diarrhea. constipation. weight loss, paralytic ilcus and dyspnca. Lesions were most frequent in thc gastrointestinal tract and lungs. In the gut thcrc wcrc erosive and ulcerative enteritis associated with adult female parasites and rhabditiform larvae and acute and granulomatous cntcrocolitis associated with invading filariform larvae. Thcrc was severe multifocal or diffuse hcmorrhagc associated with migrating larvae in the lungs of 23 gibbons. Filariform larvae and the lesions they caused also occurred in various tissues; this was commensurate with the wide distribution o f these larvae when hypcrinfcction occurred.Fatal strongyloidiasis is primarily a diseasc o f man and anthropoid apes. It is caused by the small ncmatode parasitc, Strongyloides. Strongyloides stercoralis, the prototype species and the cause of the disease in man, originally was reported [ 12) in 1876 t o be the cause of Cochin-China diarrhea, a severely debilitating and often fatal disease in French colonial soldiers on their return to France from Southeast Asia. Subsequently, cases of fatal strongyloidiasis in man have been reported from several countries including the United States. Recent fatal human cases have occurred in subclinically infected patients undergoing immunosuppressive therapy for immunologic disorders o r immunosuppressed as a result of cancer chemotherapy 13, 151.The first report of fatal strongyloidiasis in a nonhuman primate was in a chimpanzee in 1922 121. Subsequently, fatal infections with Strongyloides were reported in the gibbon (Hylobates) ( 5 , 141, the chimpanzee (Pun troglodytes) [6, I)] and the orangutan (Pungo pygmaeus)Whilst subclinical infection with Slrongyloides is not uncommon in subhuman primates [ 131, fatal infections are almost exclusive to anthropoid apes. Clinical disease and death in both apes and man arc associated with hyperinfection [4], which is the result of a unique variation in the life cycle of this parasite. Rhabditiform larvae hatched in the host's small intestine do not pass out of the' intestine to continue their life cycle but rather metamorphose while in the intestine to infective filariform larvae which then penetrate the colonic mucosa 31